ArticleOncotarget2016
Defective CFTR- β-catenin interaction promotes NF-κB nuclear translocation and intestinal inflammation in cystic fibrosis.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Review
- Distinct CFTR Mutation Spectrum and Atypical Clinical Presentations in Chinese Patients with Cystic Fibrosis.International journal of molecular sciences · 2026Review
- Bioinformatics identification of key genes correlating NOD1 and Endoplasmic Reticulum stress in Hepatitis B virus-induced acute liver failure.Scientific reports · 2025Article
- CFTR mutation is associated with bone differentiation abnormalities in cystic fibrosis.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2025Article
- Protease-activated receptor 1 in the pathogenesis of cystic fibrosis.BMJ open respiratory research · 2025Article
- Proteomics profiling of inflammatory responses to elexacaftor/tezacaftor/ivacaftor in cystic fibrosis.Frontiers in immunology · 2025Article
- Bitter taste receptor T2R14-Gαi coupling mediates innate immune responses to microbial quorum sensing molecules in cystic fibrosis.iScience · 2024Article
- Network pharmacology and anticancer mechanism study of Dendrobium nobile dendrobine in the treatment of colorectal cancer.Discover oncology · 2024Article
- Distraction Enterogenesis Induces Desert Hedgehog in the Lengthened Murine Colon.Journal of pediatric surgery · 2024Article
- Article
- Cystic fibrosis transmembrane conductance regulator prevents ischemia/reperfusion induced intestinal apoptosisWorld journal of gastroenterology · 2022Article
- Intestinal Inflammation and Alterations in the Gut Microbiota in Cystic Fibrosis: A Review of the Current Evidence, Pathophysiology and Future Directions.Journal of clinical medicine · 2022Review
- Role of inflammation and oxidative stress in tissue damage associated with cystic fibrosis: CAPE as a future therapeutic strategy.Molecular and cellular biochemistry · 2022Review
- Increased susceptibility of cystic fibrosis airway epithelial cells to ferroptosis.Biological research · 2021Article
- Article
- Functional relationship between CFTR and RAC3 expression for maintaining cancer cell stemness in human colorectal cancer.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- Bone Cells Differentiation: How CFTR Mutations May Rule the Game of Stem Cells Commitment?Frontiers in cell and developmental biology · 2021Review
- How Dysregulated Ion Channels and Transporters Take a Hand in Esophageal, Liver, and Colorectal Cancer.Reviews of physiology, biochemistry and pharmacology · 2021Review
- ABCC7/CFTR Expression Is Associated with the Clinical Course of Ulcerative Colitis Patients.Gastroenterology research and practice · 2021Article
- A Developmental Role of the Cystic Fibrosis Transmembrane Conductance Regulator in Cystic Fibrosis Lung Disease Pathogenesis.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While inflammation with aberrant activation of NF-κB pathway is a hallmark of cystic fibrosis (CF), the molecular mechanisms underlying the link between CFTR defect and activation of NF-κB-mediated pro-inflammatory response remain elusive. Here, we investigated the link between CFTR defect and NF-κB activation in ΔF508cftr-/- mouse intestine and human intestinal epithelial cell lines. Our results show that the NF-κB/COX-2/PGE2 pathway is activated whereas the β-catenin pathway is suppressed in CF mouse intestine and CFTR-knockdown cells. Activation of β-catenin pathway by GSK3 inhibitors suppresses CFTR mutation/knockdown-induced NF-κB/COX-2/PGE2 pathway in ΔF508 mouse intestine and CFTR-knockdown cells. In contrast, suppression of β-catenin signaling induces the nuclear translocation of NF-κB. In addition, CFTR co-localizes and interacts with β-catenin while CFTR mutation disrupts the interaction between NF-κB and β-catenin in mouse intestine. Treatment with proteasome inhibitor MG132 completely reverses the reduced expression of β-catenin in Caco-2 cells. Collectively, these results indicate that CFTR stabilizes β-catenin and prevents its degradation, defect of which results in the activation of NF-κB-mediated inflammatory cascade. The present study has demonstrated a previously unsuspected interaction between CFTR and β-catenin that regulates NF-κB nuclear translocation in mouse intestine. Therefore, our study provides novel insights into the physiological function of CFTR and pathogenesis of CF-related diseases in addition to the NF-κB-mediated intestinal inflammation seen in CF.
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